Amelioration of rheumatoid arthritis in rats by 4-allylanisole through modulation of inflammatory mediator

Sajida Parveen,Arham Shabbir, Adeel Masood Butt, Muhammad Imran, Anum Jamil, Ashna Asim, Kiran Mashaal

Research Square (Research Square)(2023)

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摘要
Abstract Background 4-Allylanisole, also known as Estragole (EST), is an important chemical constituent of many aromatic plants found in nature and possesses anti-inflammatory properties. Aim: Arthritic rat model induced by Freund's complete adjuvant was used to determine the anti-arthritic potential of EST in present study. Method: It was given to three groups which were administered low dose (10 mg/kg b.w.), medium dose (30 mg/kg b.w.), and of high dose (60 mg/kg b.w.). Piroxicam was used as reference drug. Arthritic score was evaluated macroscopically and through histopathological evaluation, while paw edema was evaluated using Vernier caliper. The RT-qPCR, (Real time reverse transcription polymerase chain reaction) was used to measure expression levels of pro-inflammatory mediators including interleukins (-1β) and (-6) and tumor necrosis factor. Hematological indices i.e. differential leukocyte count (DLC) and total leukocyte count (TLC), along with biochemical indices were also determined. Result: All evaluated hematological, biochemical, and histopathological parameter, as well as, mRNA expression levels of pro-inflammatory cytokines were found raised in disease control group. 4-Allylanisole significantly attenuated development of arthritis and paw edema. These results were validated by histopathological evaluation which also demonstrated amelioration of arthritis in treated groups. DLC and TLC were also nearly normalized in treatment groups. 4-allyanisole significantly attenuated the raised levels of AST, ALT, urea and creatinine. RT-qPCR analysis showed that treatment with 4-allylanisole significantly reduced TNF-α, IL-1β, and IL-6 levels. Conclusion: The results concluded that the phytochemical 4-allylanisole possesses significant anti-arthritic activity which may be attributed to down-regulation of TNF-α, IL-1β, and IL-6 levels.
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rheumatoid arthritis
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